ArticleNature genetics2017
TMPRSS2-ERG fusion co-opts master transcription factors and activates NOTCH signaling in primary prostate cancer.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
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Who cites it
130 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Dampened Regulatory Circuitry of TEAD1/ITGA1/ITGA2 Promotes TGFβ1 Signaling to Orchestrate Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Pooled it
- Androgen receptor drives divergent chromatin accessibility programs in benign and malignant prostate epithelial cells.Nucleic acids research · 2026Article
- Pioneer transcription factors direct tissue-specific cohesin chromatin entry and three-dimensional genome organization.Nature genetics · 2026Article
- Towards implementation of precision medicine biomarkers in early detection and prognostication of prostate cancer.Cancer metastasis reviews · 2026Review
- TMPRSS2-ERG confers resistance of prostate cancer to antiandrogens.EMBO molecular medicine · 2026Article
- Review
- IFDlong: a model-based isoform and fusion detector for accurate annotation and quantification of long-read RNA-seq data.Genome biology · 2026Article
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma.The Journal of clinical investigation · 2026Article
- Fusion gene discovery in single cells from high throughput long read single cell transcriptomes.bioRxiv : the preprint server for biology · 2026Article
- Epigenomics-guided precision oncology: Chromatin variants in prostate tumor evolution.International journal of cancer · 2026Review
- Prostate cancer cells converge to an inflammatory-like state upon metastatic dissemination.Nature communications · 2025Article
- Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis.Molecular oncology · 2025Article
- Reprogramming of Androgen Receptor Activity in Castration-resistant Prostate Cancer is Shaped by Truncated Variants.European urology focus · 2025Article
- ERG-driven prostate cancer initiation is cell-context dependent and requires KMT2A and DOT1L.Nature genetics · 2025Article
- DNA probe pulldown screening uncovers O-GlcNAcylation modulation of transcription factor DNA interactions.Scientific reports · 2025Article
- Role of antidiarrheal agents nifuroxazide in antitumor multi‑target anticancer, multi‑mechanism anticancer drug (Review).Oncology letters · 2025Review
- SCORT-Cas13d Nanotherapy Precisely Targets the 'Undruggable' Transcription Factor HoxB13 in Metastatic Prostate Cancer In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- VADEr: Vision Transformer-Inspired Framework for Polygenic Risk Reveals Underlying Genetic Heterogeneity in Prostate Cancer.medRxiv : the preprint server for health sciences · 2025Article
- The Germline and Somatic Origins of Prostate Cancer Heterogeneity.Cancer discovery · 2025Article
70 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TMPRSS2-ERG (T2E) structural rearrangements typify ∼50% of prostate tumors and result in overexpression of the ERG transcription factor. Using chromatin, genomic and expression data, we show distinct cis-regulatory landscapes between T2E-positive and non-T2E primary prostate tumors, which include clusters of regulatory elements (COREs). This difference is mediated by ERG co-option of HOXB13 and FOXA1, implementing a T2E-specific transcriptional profile. We also report a T2E-specific CORE on the structurally rearranged ERG locus arising from spreading of the TMPRSS2 locus pre-existing CORE, assisting in its overexpression. Finally, we show that the T2E-specific cis-regulatory landscape underlies a vulnerability against the NOTCH pathway. Indeed, NOTCH pathway inhibition antagonizes the growth and invasion of T2E-positive prostate cancer cells. Taken together, our work shows that overexpressed ERG co-opts master transcription factors to deploy a unique cis-regulatory landscape, inducing a druggable dependency on NOTCH signaling in T2E-positive prostate tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.